Evolution and host-specific adaptation of Pseudomonas aeruginosa

Author:

Weimann Aaron1234ORCID,Dinan Adam M.123ORCID,Ruis Christopher1234ORCID,Bernut Audrey5ORCID,Pont Stéphane5ORCID,Brown Karen126ORCID,Ryan Judy12,Santos Lúcia7ORCID,Ellison Louise2ORCID,Ukor Emem26ORCID,Pandurangan Arun P.189ORCID,Krokowski Sina12,Blundell Tom L.189ORCID,Welch Martin8ORCID,Blane Beth9ORCID,Judge Kim10,Bousfield Rachel911ORCID,Brown Nicholas11ORCID,Bryant Josephine M.10,Kukavica-Ibrulj Irena12ORCID,Rampioni Giordano1314ORCID,Leoni Livia13ORCID,Harrison Patrick T.7ORCID,Peacock Sharon J.911ORCID,Thomson Nicholas R.1015ORCID,Gauthier Jeff12ORCID,Fothergill Jo L.16ORCID,Levesque Roger C.12ORCID,Parkhill Julian4ORCID,Floto R. Andres12369ORCID

Affiliation:

1. Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.

2. University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.

3. Cambridge Centre for AI in Medicine, University of Cambridge, Cambridge, UK.

4. Department of Veterinary Medicine, University of Cambridge, Cambridge, UK.

5. Laboratory of Pathogens and Host Immunity (LPHI), UMR5235, CNRS/Université de Montpellier, Montpellier, France.

6. Cambridge Centre for Lung Infection, Royal Papworth Hospital, Cambridge, UK.

7. Department of Physiology, Bioscience Institute, University College Cork, Cork, Ireland.

8. Department of Biochemistry, University of Cambridge, Cambridge, UK.

9. Department of Medicine, University of Cambridge, Cambridge, UK.

10. Wellcome Sanger Institute, Hinxton, UK.

11. Cambridge University Hospitals Trust, Cambridge, UK.

12. Institut de Biologie Intégrative et des Systèmes (IBIS), Université Laval, Québec City, Québec, Canada.

13. Department of Science, University Roma Tre, Rome, Italy.

14. IRCCS Fondazione Santa Lucia, Rome, Italy.

15. London School of Hygiene and Tropical Medicine, London, UK.

16. Department of Clinical Infection, Microbiology and Immunology, University of Liverpool, Liverpool, UK.

Abstract

The major human bacterial pathogen Pseudomonas aeruginosa causes multidrug-resistant infections in people with underlying immunodeficiencies or structural lung diseases such as cystic fibrosis (CF). We show that a few environmental isolates, driven by horizontal gene acquisition, have become dominant epidemic clones that have sequentially emerged and spread through global transmission networks over the past 200 years. These clones demonstrate varying intrinsic propensities for infecting CF or non-CF individuals (linked to specific transcriptional changes enabling survival within macrophages); have undergone multiple rounds of convergent, host-specific adaptation; and have eventually lost their ability to transmit between different patient groups. Our findings thus explain the pathogenic evolution of P. aeruginosa and highlight the importance of global surveillance and cross-infection prevention in averting the emergence of future epidemic clones.

Publisher

American Association for the Advancement of Science (AAAS)

Cited by 2 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. ‘Wild Type’;Microbiology;2024-08-30

2. Mucin adhesion of serial cystic fibrosis airways Pseudomonas aeruginosa isolates;Frontiers in Cellular and Infection Microbiology;2024-08-22

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